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Recovery after cardioplegia in the hypertrophic rat heart
J A Lahorra1, D F Torchiana, C Hahn
1Department of Surgery, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.
Insights
Enhanced recovery after cardioplegic arrest in hypertrophied rat hearts is linked to increased V(3) isomyosin and glycogen, not just mass. These factors improve functional recovery and postischemic efficiency.
Area of Science:
- Cardiology
- Physiology
- Biochemistry
Background:
- Enhanced recovery after cardioplegic arrest is observed in hypertrophied rat hearts.
- This phenomenon is hypothesized to stem from altered myocardial characteristics, specifically increased V(3) isomyosin and glycolytic potential, rather than solely increased ventricular mass.
Purpose of the Study:
- To investigate the relationship between myocardial characteristics (V(3) isomyosin, glycogen content) and functional recovery after cardioplegic arrest in hypertrophied rat hearts.
- To determine if changes other than increased left ventricular mass contribute to improved recovery.
Main Methods:
- Isolated rat hearts underwent cardioplegic arrest and reperfusion.
- Hypertrophy and atrophy were induced via aortic banding, hyperthyroidism, or hypothyroidism.
- Left ventricular V(3) isomyosin percentage and myocardial glycogen content were measured.
- Functional recovery and efficiency were assessed during reperfusion.
Main Results:
- Moderate hypertrophy (aortic banding, hyperthyroidism) and atrophy (hypothyroidism) were induced.
- V(3) isomyosin and myocardial glycogen levels increased in hypertrophied and hypothyroid hearts.
- Hearts from banded and hypothyroid rats showed significantly improved functional recovery (80-81%) and efficiency post-arrest compared to controls (66-68%).
Conclusions:
- Improved recovery after cardioplegic arrest in overload hypertrophy is associated with increased V(3) isomyosin and glycogen, not solely increased mass.
- These molecular and metabolic changes may directly contribute to enhanced functional recovery and postischemic efficiency.
Background:
Enhanced recovery after cardioplegic arrest has been observed in rat hearts with hypertrophy induced by hemodynamic overload. We hypothesize that this is related to altered characteristics of hypertrophied myocardium-reflected by increased V(3) isomyosin and glycolytic potential-other than increased left ventricular mass.
Materials And Methods:
Isolated hearts from age-matched nonoperated and sham-operated control rats and from aortic-banded, hyperthyroid, and hypothyroid rats-groups in which hypertrophy and V(3) as a percentage of left ventricular myosin vary independently-underwent 2 h of multidose cardioplegic arrest at 8 degrees C followed by reperfusion at 37 degrees C. Left ventricular V(3) isomyosin was evaluated after separation by gel electrophoresis.
Results:
Moderate left ventricular hypertrophy was produced by aortic banding or hyperthyroidism and atrophy by hypothyroidism. V(3) isomyosin was increased in banded (28%) and hypothyroid (75%) rats compared to control (12%) and hyperthyroid rats (7%). Myocardial glycogen content closely paralleled %V(3). At 30 min of working reperfusion, functional recovery (assessed as percentage prearrest cardiac output) was 66 +/- 4 and 68 +/- 5% in control and hyperthyroid hearts and 81 +/- 2 and 80 +/- 5% in hearts from banded and hypothyroid rats (each P < 0.05 vs controls), respectively. At 30 min, hearts from banded and hypothyroid rats were also more efficient (as indexed by cardiac output at constant mean aortic pressure/myocardial oxygen consumption) than control and hyperthyroid hearts.
Conclusions:
The data suggest that recovery is related not to increased mass but to other changes in overload hypertrophy. Increased percentage V(3) isomyosin and glycogen reflect these changes and may themselves contribute to improved functional recovery after cardioplegic arrest, as may increased postischemic efficiency.
